By Negus, David
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Additional resources for Leg Ulcers 3Ed: Diagnosis and management
Varicose veins in women cotton workers. An epidemiological study in England and Egypt. Br Med J 1969; 2: 591–5. 10. Malhotra SL. An epidemiological study of varicose veins in Indian railroad workers from the south and north of India, with special reference to the causation and prevention of varicose veins. Int J Epidemiol 1972; 1: 117–83. 11. Guberan W, Widmer LK, Glaus L, Muller R et al. Causative factors of varicose veins: myths and facts. Vasa 1973; 2: 115–20. 12. Coon WW, Willis PW, Keller JB.
34. Cornwall JV, Doré CJ, Lewis JD. Leg ulcers: epidemiology and aetiology. Br J Surg 1986; 73: 693–6. 35. Henry M. Incidence of varicose ulcers in Ireland. Ir Med J 1986; 79: 65–7. 36. Baker SR, Stacey MC, Singh G, Hoskin SE et al. Aetiology of chronic leg ulcers. Eur J Vasc Surg 1992; 6: 245–51. 37. Nelzén O, Bergqvist D, Lindhagen A, Hallböök T. Chronic leg ulcers: an underestimated problem in primary health care among elderly patients. J Epidemiol Community Health 1991; 45: 184–7. 38. Lindholm C, Bjellerup M, Christensen OB, Zederfeldt B.
5a). When the calf muscles contract, distal ﬂow down the great saphenous vein continues, but proximal ﬂow along the distal posterior arch vein, which is already distended to its elastic limit, is opposed by an outward pressure of 140 mmHg transmitted through the deep fascia from the deep veins by an incompetent perforating vein (Fig. 5b). The resulting high pressure and ﬂow are transmitted through the tributaries of the posterior arch vein, which dilate to form the corona phlebectatica. The high venous pressure and ﬂow in this venous network are then transmitted to the venules which drain the skin capillaries and these dilate and elongate, resulting in the microcirculatory changes which underlie lipodermatosclerosis and ulceration.